Monthly Archives: March 2015

Under normal conditions of exercise the body has two main sources of fuel: fat and carbohydrate (CHO). The According to Jeukendrup 2003, the body has roughly 2000 kcal of stored CHO, stored primarily as muscle glycogen. If we assume that an average person would expend ~100 kcal per mile of running, then this would translate to ~20 miles of running(Jeukendrup, 2003). In contrast, the Jeukendrup 2003 reports that the human body stores roughly 106,000 kcal of fat, primarily in adipocytes (100,000 kcal) and secondarily as intramuscular triacylglyceride (2600 kcal) (Jeukendrup, 2003). Theoretically, there are several possible benefits to increasing reliance on fat oxidation. As previous research has shown that glycogen availability may impact force generation by modulating sarcoplasmic reticulum (SR) calcium release (Ørtenblad, Nielsen, Saltin, & Holmberg, 2011), sparing muscle glycogen by oxidizing more fat may preserve force generation. In order to be metabolized, fat is mobilized from triglyceride storage and delivered to the mitochondria as free fatty acids (Horowitz & Klein, 2000). Fatty acids are then broken into 2 carbon fragments in the form of acylCoa. During this process one FADH and one NADH are generated, but no direct rephosphorylation of ADP to ATP occurs. Unlike oxidation of glucose, fat oxidation requires more flux through the oxidative pathways since generation of ATP is nearly exclusively through the electron transport chain (ETC) (Gropper & Smith, 2012). Since there increased flux through ETC there may be a training effect to increasing reliance on fat as a fuel source (Miller, Bryce, & Conlee, 1983; Simi, Sempore, Mayet, & Favier, 1991).

Several studies on rats have provided encouraging data that high fat diets may improve endurance capacity through stimulating increases in oxidative enzymes and preservation of muscle glycogen stores (Conlee et al., 1990; Miller et al., 1983; Simi et al., 1991). Miller et al., 1983 showed that a high fat diet reduced muscle glycogen and liver stores, but also improved exercise capacity and oxidative enzymes (Miller et al., 1983). Simi et al., 1991 provided evidence that while training may blunt this effect, there is still an effect on oxidative capacity for a high fat diet after training in rats. However, it is possible this effect could disappear if the training stimulus were high enough since the training stimulus used was quite small (Simi et al., 1991). Conlee et al., 1990 may suggest there is added benefit to fat adapting a rat and then transiently increasing CHO prior to exercise (Conlee et al., 1990).

It is important to understand that while these results are encouraging, human studies have had less positive results (Horvath, Eagen, Fisher, Leddy, & Pendergast, 2000; Rowlands & Hopkins, 2002; Vogt et al., 2003). This may be in part due to the large variation in diets deemed high fat in human studies. The animal studies tended to have fat intakes around 70% of the diet, whereas high fat diets in human studies have ranged from 44-70%. It appears there may be two defined diets based on the literature. The first diet deemed high fat is based on increasing fat intake beyond the recommended 20-35% of calories (“Nutrition and Athletic Performance,” 2009). These diets tend to have a higher proportion of fat, but maintain a substantial contribution from carbohydrates (Horvath et al., 2000; Rowlands & Hopkins, 2002; Vogt et al., 2003). The other version of the high fat diet is additionally very low carbohydrate (Goedecke et al., 1999; Lambert, Speechly, Dennis, & Noakes, 1994). Such a large range of diets classified as high fat may be partly responsible for the mixed results. In support of this, Lambert et al., 1994 found that a diet of 70% fat significantly improved time to exhaustion at 60% of VO2max. However, time to exhaustion at 90% VO2max and CHO oxidation rates at high intensity were unaltered (Lambert et al., 1994). Goedecke et al 1999 used a high fat diet, 69 ± 1% fat, for 15 days (Goedecke et al., 1999). Carnitine acyl transferase activity was significantly increased within 5-10 days of being fed a high fat diet. However, 40 km cycling time trial performance was not significantly different compared with a high carbohydrate diet. Taken together, it appears that a high fat, low carbohydrate diet may have beneficial effects at moderate intensity activities, but when intensity is increased beyond a certain threshold, the working muscles will still shift to burning almost exclusively carbohydrate. After this shift occurs, there is likely no performance benefit to a high fat diet.

Early studies on high fat diets focused on the metabolic consequences of such diets which were shown to induce obesity in animal models (Mašek & Fabry, 1959). In fact, a number of studies have shown that high fat diets can induce metabolic syndrome and insulin resistance (Ikemoto et al., 1996; Oakes, Cooney, Camilleri, Chisholm, & Kraegen, 1997; Todoric et al., 2006; Tschöp & Heiman, 2001). However, it should be noted that the type of fat used in the diet can have an impact on this outcome. Particularly, Ikemoto et al. 1996 found there was a positive association between linoleic acid intake and plasma glucose, and that a diet high in fish oil actually had beneficial effects on body weight and glucose uptake. Other studies have suggested there is a beneficial effect on health for diets high in fish oil (Buettner et al., 2006). It appears there may be a gap in the literature on the long term consequences of high fat diets in combination with endurance exercise. In light of this, it would be prudent to recommend athletes attempting to alter substrate utilization through a high fat diet should consume most of their fats from sources shown to not adversely affect glucose uptake.

Literature on high fat diets and exercise performance that account for types of fat seem to be scarce. However, there have been a number of experiments examining medium chain fatty acids as a potential energy source during exercise. Medium chain fatty acids are described as fatty acids with 6-10 carbons that readily cross the mitochondrial membrane where medium chain acyl CoA synthases activate them before they are oxidized (Marten, Pfeuffer, & Schrezenmeir, 2006). The rationale would be to supplement with the medium chain fatty acids just prior to or during exercise to provide an energy source during exercise (Angus, Hargreaves, Dancey, & Febbraio, 2000; Jeukendrup, Saris, Schrauwen, Brouns, & Wagenmakers, 1995). However, as pointed out by Jeukendrup et al. 1995, the GI tract has a low tolerance for medium chain fatty acids during exercise, which may limit its usefulness as an ergogenic aid.

It is currently unclear why someone might recommend a high fat diet for strength performance. Anecdotally, numerous books promote “paleo” diets which tend to be low carbohydrate, higher fat, for numerous athletic populations (Burnett, 2012; Outram, 2014; Smith, 2012). Many of these books claim that humans evolved to eat only meat based on little or no actual research. However, some studies have attempted to examine early human diets, but found that early humans likely ate a mixed diet with slightly increased protein and decreased fat intake (Nestle, 2000), while other studies contradict this finding suggesting diets were high in fat and low to moderate in carbohydrate (Eaton & Eaton Iii, 2000). Studies on modern indigenous tribes suggest there may also be a larger role for dietary fiber for such populations (Johns, Nagarajan, Parkipuny, & Jones, 2000). It may be that early humans had a large range of diets depending upon food availability and regional culture. It should also be noted that it is currently unclear whether early humans were any healthier due to their diets (Nestle, 2000). One study suggests that the stereotypical “caveman” diet would be lethal to pregnant women and their fetuses (Hockett, 2012), suggesting that these diets may differ from popular conception. It appears there is very little literature on using a high fat diet to improve performance for strength athletes. However, high fat meals have been shown to reduce total and free testosterone (Cano et al., 2008; Volek, Love, Avery, Sharman, & Kraemer, 2001), but it is unclear whether these reductions in androgens would be large enough to affect adaptation to strength training.